The objective of this study will be to define new factors of adrenocortical origin in human hypertensive disease. Efforts will be concentrated in a juvenile hypertensive syndrome resembling primary aldosteronism but with subnormal production of all known steroids. An abnormality has been detected in these patients consisting of a defect in the reductive metabolism of the steroid ring A, with accumulation of corticosteroid 4,5-dihydro metabolites, and the excretion of 3-keto metabolites in the urine in unconjugated form. A second aspect of the defect is an abnormal predominance of 5 alpha-dihydro epimers relative to the 5 beta forms. Preliminary results indicate that the mineralocorticoid activity of 5 alpha-dihydrocortisol may be an etiologic factor in the hypertension of these patients. A second abnormality in some patients consists of a much decreased ratio of 11-keto to 11 beta-hydroxy steroid metabolites due to reduced activity of the 11 beta-hydroxy oxidoreductase system and shift in the cortisol yields (reversibly) cortisone equilibrium in favor of cortisol. These biochemical abnormalities will be sought in hypertensive patients.